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Where To Buy Stearic Acid Locally

Our Stearic Acid is triple pressed palm stearic acid. This product is cosmetic grade. Stearic Acid is commonly used to emulsify lotions made from scratch. It can also be used in candle manufacturing to raise the melt point and improve the hardness of candle wax along with countless other applications.

where to buy stearic acid locally

When it comes to cosmetics, stearic acid in skin care is used to provide a stable base for a range of products but also to bind and thicken certain formulations. And stearic acid in skin care is commonly used as a rust removal and oxidisation prevention measure. Iron and aluminium containers are often coated with stearic acid in skin care products so they can be stored longer with minimal possibility of rusting. Stearic acid in soapmaking is used to harden soaps and provide shampoos with a pearly white shine during the process. Stearic acid in candlemaking is used to harden the wax and make the candle stronger.

Stearic acid uses its properties to provide actual skin benefits and not just on the products alone. Plus, the versatility of stearic acid in skin care makes it a popular ingredient in plenty of applications!

Whether you want to use stearic acid in skin care, or whatever you need it for, always acquire it from a trusted supplier. Thankfully, you can buy it online at N-essentials! Purchase from our online shop now and enjoy essential perks! Feel free to contact us regarding prices and bulk orders.

Hydroxyl fatty acids and their derivatives are of high value due to their wide range of industrial application, including cosmetic, food, personal care and pharmaceutical products. Realizing the importance of hydroxyl fatty acids, and yet due to the absence of the conventional starting raw materials, Malaysia has developed 9,10-dihydroxystearic acid (9,10-DHSA) and its derivatives from locally abundant palm based oils. The aim of this article is to provide a general description of the works that have thus far being done on palm based 9,10-DHSA: starting from its conception and production from commercial grade palm based crude oleic acid via epoxidation and hydrolysis, purification through solvent crystallization and characterization through wet and analytical chemistry, moving on to developmental works done on producing its derivatives through blending, esterification, amidation and polymerization, and completing with applications of 9,10-DHSA and its derivatives, e.g. DHSA-stearates and DHSA-estolides, in commercial products such as soaps, deodorant sticks and shampoos. This article incorporates some of the patent filed technological knowhow on 9,10-DHSA and its derivatives, and will also point out some of the shortcomings in previously published documents and provide some recommendations for future research works in mitigating these shortcomings.

Furthermore, we confirmed the involvement of TRIF in this priming effect of stearic acid using small molecule (Resveratrol) inhibitor. Pretreatment of monocytic cells with resveratrol abrogated the cooperative actions of stearic acid on the TNF-α mediated production of MIP-1α/CCL3 (Figure 3E,F). Similarly, inhibiting the TBK1 adaptor protein with BX795 attenuates the cooperative effect of stearic acid on MIP-1α/CCL3 production (Figure 3G,H).

Next, we verify that the cooperative effect of stearic acid on TNF-α mediated production of MIP-1α/CCL3 was dependent on the TLR4-IRF3 signaling axis. THP-1 Monocytic cells were transfected with Irf3 siRNA and scrambled siRNA control (Figure 4A). Cooperative effect of stearic acid/TNF-α on MIP-1α/CCL3 production was significantly reduced in the IRF3 deficient THP-1 cells (Figure 4B,C). IRF3 reporter cells showed that stearic acid enhances the IRF3 activity (Figure 4D). Western blot analysis showed that stearic acid induced IRF3 phosphorylation in a time-dependent manner, verifies the role of IRF3 in the cooperative effect of stearic acid for TNF-α mediated production of MIP-1α/CCL3 (Figure 4E).

Stearic acid cooperative effect with TNF-α for MIP-1α/CCL3 production requires IRF3. (A) THP-1 monocytic cells were transfected with either control or IRF3 siRNA and incubated for 36 h. Real time PCR was done to measure IRF3 expression. (B,C) IRF3 deficient THP-1 cells were stimulated with stearic acid and TNF-α. MIP-1α/CCL3 expression was determined. The results obtained from minimum three independent experiments with three replicates of each experiment are shown. (D) IRF3 activity reporter monocytic cells were treated with stearic acid (200 µM) or 0.1% BSA (control) or TNF-α (10 ng/mL) or in combination. Culture media were collected after 24 h. Cell culture media were assayed for luciferase activity representing the degree of IRF3/ISRE activation using Quanti-Luc medium. (E) Western blot analysis showed that stearic acid induced IRF3 phosphorylation in a time dependent manner in THP-1 monocytes, verifies the role of IRF3 in the cooperative effect of stearic acid in the TNF-α mediated production of MIP-1α/CCL3. (F) Expression of phosphorylated IRF3 is shown as determined by densitometry of western blot bands. * P

IRF3 is one of the major effectors of TLR4-MyD88 independent signaling pathway. Activation of IRF3 upregulates the expression of interferons and several inflammatory genes [47,48,49]. Our result showed that IRF3 deficiency significantly blocks the cooperative effect of stearic acid. Furthermore, IRF3 activation by poly-IC mimics the cooperative effect of stearic acid on the production of MIP-1α/CCL3 by TNF-α. Individuals with obesity have elevated levels of stearic acid along with other fatty acids. We found that individuals with obesity have a high expression of p-IRF3 compared to lean individuals, suggesting that plasma free fatty acids in individuals with obesity contribute to the activation of proinflammatory genes regulated under the influence of IRF3. Overexpression of IRF3 in the adipocytes in both human and mouse obesity has been reported. It was shown that activation of TLR4/IRF3 signaling pathways results in insulin resistance in murine adipocytes. Furthermore, mice lacking IRF3 are protected from diet-induced insulin resistance and systemic inflammation. Thus, IRF3 deficiency enhances the browning of subcutaneous fat along with increased adipose expression of GLUT4 [28]. These data confirm the role of IRF3 as a primary transcriptional regulator involve in adipose tissue inflammation, maintaining systemic glucose, and energy homeostasis. Our data show that stearic acid/TNF-α synergy involves the NF-κB/AP-1 mediated signaling. However, it is also plausible that stearic acid accumulation in macrophages may trigger inflammation independent of TLR4 involvement via the ER/oxidative stress [50].

The following are available online at -9059/8/10/403/s1, Figure S1: Dose dependent manner of cooperative effect of stearic acid on TNF-α mediated MIP-1α/CCL3 production. Table S1: Characteristics of the study participants title.

In comparison, paraffin wax candles are made from petroleum, a non-renewable resource. Petroleum undergoes several chemical processes, along with the addition of stearic acid and synthetic fragrance before it becomes paraffin. When burned paraffin releases toxins from these chemical processes and additives into the air.

The Stearic-PEI600 was synthesized according to a previous report described by Wan et al[28]. In brief, 0.35 g (2.16 mmol) N, N'-carbonyldiimidazole (CDI) was dissolved in 10 ml anhydrous chloroform. 0.6 g (2.1 mmol) stearic acid was dissolved in dry chloroform (10 ml) and then added dropwise into upper CDI solution under magnetic stirring. The mixture was reacted at room temperature for 2 h under argon protection. The activated stearic acid was further added drop by drop to the dry branched PEI solution (0.7 g, 1.17 mmol, in 20 ml dry chloroform). The suspension was kept stirring at room temperature for further 24 h under argon protection. The resulting product was purified by precipitation in cold ether and collected by centrifuge at 3000 rpm for 10 min. The purified Stearic-PEI600 was further dried under high vacuum condition to remove trace amount of solvent.

The stearic acid modified polyethylenimine 600 (Stearic-PEI) polymer was synthesized. The resulting Stearic-PEI, combined with DSPC and DSPE-PEG2k, was used to fabricate the cationic MBs. The PEI endows the cationic MBs with more amino groups to couple DNA than plain MBs.

It is notable that a significant improvement of DNA loading capacity was achieved in our new designed cationic MBs. The improvement of DNA loading capacity may contribute to the abundant amino group in PEI molecules. Each PEI600 molecule has approximately 14 nitrogen atoms, and at most 12 residual nitrogen atoms of which could be protonated to adsorb DNA after being modified by two stearic acid molecules. So, ideally, the maximum DNA loading capacity should be ten folds more than that of the traditional cationic MBs which consist of the same molar ratio of polymers such as DSTAP. Herein, DNA loading capacity of PEI600 MB we measured is about five times higher than that of the reported DSTAP MBs, which may be because of the steric hindrance. Borden et al. applied a layer-by-layer (LBL) assembly technique to adsorb multiple layers of DNA and poly-L-lysine (PLL) onto lipid-coated MBs [30]. The DNA loading capacity was enhanced by over 10-fold by using five paired layers. Nevertheless, LBL assembly technique is somewhat complex as the fragility of the MBs.

The worldwide prevalence of type 2 diabetes mellitus (T2DM) has grown over the past three decades and continues to do so. It is characterized by insulin resistance and progressive failure of pancreatic β-cells (Smyth & Heron 2006, Li et al. 2012, GBD et al. 2016, Chen et al. 2017). Chronic exposure to elevated saturated fatty acid (SFA) is a major risk factor for β-cell dysfunction that can accelerate the progression of T2DM (Welsh et al. 2005, Risérus et al. 2009, Giacca et al. 2011). SFA, including palmitic acid (C16:0) and stearic acid (C18:0), exerts deleterious effects on β-cells (Listenberger et al. 2003, Elsner et al. 2011). Palmitic acid has long been thought to be a major regulator of β-cell function; however, emerging evidence indicates that stearic acid also plays a critical role in β-cell dysfunction (Šrámek et al. 2017, Acosta-Montaño et al. 2019, Nemecz et al. 2019). We previously found that, compared with other non-esterified fatty acids (NEFAs), only stearic acid levels were dramatically increased in the postprandial serum of T2DM patients or in high-fat diet fed mice (Chu et al. 2013, Lu et al. 2016b). Meanwhile, high levels of stearic acid have a strong destructive effect on β-cells, stronger than that of palmitic acid (Lu et al. 2016a,b, 2018). Although generating endoplasmic reticulum (ER) stress (Lu et al. 2016a), alterations in calcium homeostasis (Marafie et al. 2019) and mitochondria dysfunction (Gehrmann et al 2010) have been reported to be involved in the stearic-acid-induced lipotoxicity to pancreatic β-cells, and its precise cellular and molecular mechanisms are complex and still need to be further elucidated. 041b061a72


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